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Causes of Contact dermatitis

List of causes of Contact dermatitis

Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Contact dermatitis) that could possibly cause Contact dermatitis includes:

Contact dermatitis Causes: Book Excerpts

Contact dermatitis as a symptom:

Conditions listing Contact dermatitis as a symptom may also be potential underlying causes of Contact dermatitis. Our database lists the following as having Contact dermatitis as a symptom of that condition:

Medications or substances causing Contact dermatitis:

The following drugs, medications, substances or toxins are some of the possible causes of Contact dermatitis as a symptom. This list is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.

See full list of 59 medications causing Contact dermatitis


What triggers Contact dermatitis?

The following conditions are listed as possible triggers for Contact dermatitis:

Related information on causes of Contact dermatitis:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of Contact dermatitis may be found in:

Causes of Contact dermatitis: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Contact dermatitis.

Atopic dermatitis: Causes
(Professional Guide to Diseases (Eighth Edition))

The cause of atopic dermatitis is still unknown. However, several theories attempt to explain its pathogenesis. One theory suggests an underlying metabolically or biochemically induced skin disorder that’s genetically linked to elevated serum immunoglobulin (Ig) E levels. Another theory suggests defective T-cell function.

Exacerbating factors of atopic dermatitis include irritants, infections (commonly caused by Staphylococcus aureus), and some allergens. Although no reliable link exists between atopic dermatitis and exposure to inhalant allergens (such as house dust and animal dander), exposure to food allergens (such as soybeans, fish, or nuts) may coincide with flare-ups of atopic dermatitis.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Dermatitis: Causes and incidence
(Professional Guide to Diseases (Eighth Edition))

The cause of atopic dermatitis is unknown, but a genetic predisposition may be exacerbated by such factors as food allergies, infections, irritating chemicals, temperature and humidity, and emotions. Approximately 10% of childhood cases are due to allergy to certain foods, particularly eggs, peanuts, milk, fish, soy, and wheat. Atopic dermatitis tends to flare up in response to extremes in temperature and humidity. Other causes of flare-ups are sweating and psychological stress.

An important secondary cause of atopic dermatitis is irritation, which seems to change the epidermal structure, allowing immunoglobulin (Ig) E activity to increase. Consequently, chronic skin irritation usually continues even after exposure to the allergen has ended or after the irritation has been systemically controlled.

Atopic dermatitis is most common in infants, usually developing between ages 1 month and 1 year, commonly in those with strong family histories of atopic disease. At least half of those cases clear by age 36 months. These children often acquire other atopic disorders as they grow older. Typically, this form of dermatitis flares and subsides repeatedly before finally resolving during adolescence. However, it can persist into adulthood. In adults, it’s generally chronic or recurring.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Diseases (Eighth Edition), 2005

Arthritis/Dermatitis: Differential Overview
(Field Guide to Bedside Diagnosis)

❑Lyme disease

❑Erythema nodosum

❑Rheumatoid arthritis

❑Systemic lupus erythematosus

❑Psoriatic arthritis

❑Disseminated gonococcemia

❑Sarcoidosis

❑Scleroderma

❑Dermatomyositis

❑Reiter syndrome

❑Rheumatic fever

❑Behçet syndrome

❑Still disease

❑Hypersensitivity vasculitis

Clinical Findings

Lyme disease  Erythema migrans, a rapidly expanding annular rash with a clearing center, is the key early finding. The site of the ixodid tick bite at the center of the lesion is usually intensely indurated, vesicular, or necrotic. The arthritis is an asymmetric oligoarthritis that usually occurs after the rash has resolved.

Erythema nodosum  A prodromal syndrome of fever, chills, malaise, and polyarthralgia is followed by the development of lesions that are discrete, tender, slightly raised subcutaneous nodules on the shins or ankles. They represent a hypersensitivity reaction to group A streptococcal infection, tuberculosis, sarcoidosis, inflammatory bowel disease, or drugs such as oral contraceptives and sulfonamides.

Rheumatoid arthritis  Symmetric polyarticular arthritis with synovial proliferation, especially of the wrist, and morning stiffness lasting more than 1 hour characterize the early joint involvement. Rheumatoid nodules appear over extensor surfaces. Vasculitic lesions are frequently found on the digits, appearing as small red or purpuric macules that progress to painful nodules or ulcers.

Systemic lupus erythematosus  A classic butterfly rash occurs in 40% and is exacerbated by sun exposure. A diffuse maculopapular rash in areas exposed to the sun heralds disease flares. Discoid lesions and scaling plaques that range in color from red to violaceous, with central atrophy and telangiectasias, occur in 20%. Vasculitis, in the form of painful ulcers on the extremities, palpable purpura, or lupus profundus (firm nodules in the subcutaneous fat on the forehead, cheeks, buttocks, and upper arms) are found. The arthritis is typically one of symmetric fusiform swelling of the proximal interphalangeal and metacarpophalangeal joints, diffuse puffiness of the hands, and tenosynovitis.

Psoriatic arthritis  Psoriatic plaques, erythematous with a silvery scale, are critical to diagnosis, but may be hidden in the scalp, umbilicus, or gluteal folds. Nail changes such as pitting or yellow discoloration of the nail plate are other clues. The arthritis typically involves the proximal interphalangeal and distal interphalangeal joints, creating sausage digits. The arthritis may become erosive, leading to telescoping of the hands. One-fourth of patients have axial skeletal arthritis.

Disseminated gonococcemia  Acral lesions are typically hemorrhagic pustules, but petechiae, hemorrhagic papules, or hemorrhagic bullae can occur. Fever, rigor, tenosynovitis, and polyarthritis are other findings.

Sarcoidosis  Transient maculopapular eruptions of the trunk, face, and extremities are often accompanied by uveitis, adenopathy, and parotid enlargement. Translucent reddish-brown to purple indolent plaques may develop on the face (lupus pernio), buttocks, or extremities. Joint symptoms consist of migratory transient arthralgias.

Scleroderma  Early findings are primarily Raynaud phenomenon and puffy fingers. Later findings include sclerodactyly (smooth, shiny, tapered fingers with taut, bound-down skin); contractures with “claw hand” deformity; expressionless face (with thin lips, a beak-like nose, and sunken cheeks); microstomia; mat telangiectasias on the nail folds, face, lips, oral mucosa, or trunk; and calcinosis with leathery crepitation over the joints.

Dermatomyositis  The classic skin manifestation is a lilac-colored heliotrope rash on the eyelids and in a butterfly distribution. Gottron papules are violaceous, scaly, flat lesions on the extensor aspect of the interphalangeal joints, elbows, knees, and medial malleoli; these occur as a late manifestation. Proximal muscle aching/weakness, not arthritis, is prominent. The patient is unable to reach overhead or arise from a chair. Neck flexors are more involved than extensors.

Reiter syndrome  Arthritis, urethritis, conjunctivitis, and mucocutaneous ulcers are found. The arthritis is asymmetric, usually involving the lower extremity joints. Solitary sausage digits may be seen. Tendinitis and fasciitis are common. The mucocutaneous lesions are eroded red vesicles or papules of the corona and glans, which when confluent are called circinate balanitis. Pustules may change into thick hyperkeratotic plaques on the palms and soles, keratoderma blennorrhagicum.

Rheumatic fever  There is an acute migratory polyarthritis with fever. Subcutaneous nodules appear over the bony prominences of the elbows, knuckles, ankles, scapulae, and occiput. They are associated with carditis. Erythema marginatum, appearing as evanescent pink lesions with serpiginous borders, is also associated with carditis.

Behçet syndrome  The classic triad is arthritis, iritis, and oral and genital ulcerations. Recurrent aphthous ulcers are a sine qua non. They begin as macular erythema that develops into superficial gray ulcers. Scrotal or labial ulcerations are also found. Hypopyon uveitis, a hallmark, is a rare finding. The arthritis is primarily of the knees and ankles.

Still disease  Skin lesions are red, flat, and less than 1 cm in diameter. Lesions are evanescent, occurring with fever spikes. A migratory polyarthralgia occurs.

Hypersensitivity vasculitis  After an upper respiratory infection, young adults may develop palpable purpura over the extensor surfaces and buttocks. Arthritis, edema, and colicky abdominal pain, followed by bloody stools, suggests the diagnosis.

» READ BOOK EXCERPT ONLINE »

Source: Field Guide to Bedside Diagnosis, 2007

Dermatitis: Causes
(Handbook of Diseases)

The cause of atopic dermatitis is unknown, but there is a genetic predisposition exacerbated by such factors as food allergies, infections, irritating chemicals, temperature and humidity, and emotions. Approximately 10% of childhood cases are caused by allergy to certain foods, particularly eggs, peanuts, milk, and wheat.

Atopic dermatitis tends to flare up in response to extremes in temperature and humidity. Other causes of flare-ups are sweating and psychological stress.

An important secondary cause of atopic dermatitis is irritation, which seems to change the epidermal structure, allowing immunoglobulin (Ig) E activity to increase. Consequently, chronic skin irritation usually continues even after exposure to the allergen has ended or after the irritation has been systemically controlled.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Contact Dermatitis: Contact Dermatitis - risk factors
(The 5-Minute Pediatric Consult)

  • Susceptibility to certain contact allergens for delayed hypersensitivity is in part genetically determined.
  • It is unclear whether atopic dermatitis is associated with an increased risk of developing contact dermatitis.
  • Increased exposure to potential allergens and the chronic or intermittent development of an impaired skin barrier are predisposing factors.

Contact Dermatitis - pathophysiology

  • Allergic contact dermatitis requires initial exposure and sensitization to an allergen and only occurs in susceptible individuals. Repeated exposure to the allergen leads to the development of a T-cell mediated delayed-type hypersensitivity reaction.
  • Irritant contact dermatitis does not involve an immunologic response and can occur in anyone, even after the 1st exposure to the irritant. It commonly results from frequent or chronic exposure to moisture and/or friction such as from water, saliva, or urine or to acidic or alkaline chemicals such as soaps and detergents.
  • Both processes result in nonspecific findings of dermal and epidermal edema and inflammation, and may be indistinguishable from other forms of eczematous dermatitis.

Contact Dermatitis - etiology

  • Irritant contact dermatitis:
    • Frequent handwashing or water immersion
    • Soaps and detergents
    • Saliva (lip licking)
    • Urine and feces (diaper dermatitis)
  • Allergic contact dermatitis:
    • Nickel and other metals
    • Fragrances (e.g., Balsam of Peru)
    • Clothing dyes
    • Formaldehydes
    • Lanolin
    • Topical antibiotics (neomycin, bacitracin)
    • Rubber and rubber accelerators
    • Plants (Toxicodendron species, e.g., poison ivy, poison oak, and poison sumac, which contain the allergen urushiol)

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Symptoms of Contact dermatitis

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